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Query: UMLS:C0024530 (malaria)
 44,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To study the risk factors for Plasmodium vivax gametocyte carriage, the presence or absence of gametocytes was determined in 2,125 patients with P. vivax malaria participating in clinical trials at the Hospital for Tropical Diseases in Bangkok, Thailand. Stepwise logistic regression models were used to determine which variables were significantly related to gametocyte carriage. On admission, 615 patients (29%) had detectable gametocytes (before treatment). After treatment had started, an additional 245 patients (11%) developed patent gametocytemia. The variables retained by multivariate analysis were highest observed temperature (adjusted odds ratio [AOR] per degrees C increase = 0.82, 95% confidence interval [CI] = 0.71-0.94, P = 0.006), asexual parasitemia > 9,200/muL (AOR = 2.8, 95% CI = 1.9-4.2, P < 0.0001), erythrocyte counts (AOR = 0.8/million/muL increase, 95% CI = 0.67-0.95, P = 0.01), monocyte percentage (AOR = 0.93 per % increase, 95% CI = 0.89-0.96, P < 0.0001), lymphocyte percentage (AOR = 0.98 per % increase, 95% CI = 0.97-0.99, P = 0.006), albumin (AOR = 0.67 per 10 g/mL increase, 95% CI = 0.5-0.9, P = 0.007), and anion gap (AOR = 1.1 per unit increase, 95% CI = 1.02-1.14, P = 0.009). The possible significance of these observations is discussed.
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PMID:Risk factors for Plasmodium vivax gametocyte carriage in Thailand. 1564 56

Data on the effects of Plasmodium gallinaceum on domesticated fowl are sparse, justifying a full investigation of its pathology. Clinical signs following blood-induced infections with the Wellcome line of strain 8A included depression, fever, anorexia, reduced weight gain, poor feed conversion, anaemia, green faeces and often death. After administration of 10(6) erythrocytic parasites, mortality 5 to 10 days after infection was 10% to 93% in chickens 7 to 84 days old. The older the birds, the lower the mortality and the longer the time to death. Onset of detectable parasitaemia occurred mostly during the second day after infection (59% of birds). Peak parasitaemia (approximately 70%) occurred on the sixth day in 85% of surviving birds. The patent period was usually 7 to 19 days. Abnormally low haematocrit values of < or =24% and high colonic temperatures of > or =42 degrees C were recorded. A febrile response is demonstrated conclusively here in P. gallinaceum malaria for the first time. Weight gain of malarious birds was reduced by approximately 18% to 51%, and feed conversion efficiency was often reduced by approximately 12% to 41%. Growth reduction was due entirely to anorexia. Liver weight relative to body weight (normally approximately 2% to 3%) increased to approximately 4.5% by 8 days, and relative spleen weight (normally approximately 0.2%) increased to 1.6% by 12 days. Specific gravities of livers and spleens in healthy and infected birds were approximately 1.09. Gall bladder volume in malarious birds 8 days after infection was approximately four times that of normal birds. Statistically significant changes occurred in the proportions of plasma proteins in malarious birds 8 days after infection; albumin and alpha2-globulin were reduced, while gamma1-globulin and gamma2-globulin were increased. Those changes coincided with significant increases in concentrations of plasma total protein and the enzymes aspartate aminotransferase, glutamate dehydrogenase and gamma-glutamyltransferase, and a decrease in creatinine. Green (biliverdin) colouration of the faeces was a consistent sign of malaria. Birds acquired non-sterile immunity after a single primary infection. The quantitative data presented facilitate selection of the most useful criteria for field diagnosis, estimation of potential economic losses, and assessment of potential avian antimalarial drugs.
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PMID:Avian malaria: clinical and chemical pathology of Plasmodium gallinaceum in the domesticated fowl Gallus gallus. 1576 37

The aim of the present study is to evaluate the status of plasma essential trace elements selenium (Se), zinc (Zn), copper (Cu), and iron (Fe) concentrations and their related acute-phase proteins, ceruloplasmin (Cp), ferritin, transferrin (Tf), and albumin levels in patients with vivax malaria. Plasma Cu and Zn concentrations were determined by atomic absorption spectrometry (AAS). Se concentrations were determined by graphite furnace AAS. Fe, Cp, Tf, and albumin levels were determined by colorimetric methods. Plasma Se, Fe, and albumin levels were found to be significantly lower (p < 0.01, p < 0.001, and p < 0.05, respectively) and Cu, Cp, and ferritin levels and Cu/Zn ratios were significantly higher (p < 0.001, p < 0.001, p < 0.001, and p < 0.05, respectively) in patients when compared with those of healthy subjects. Plasma, Tf, and Zn levels were not found to be significantly different (p > 0.05) in patients and controls. There were positive important correlations between Cu and Cp (r = 0.908, p < 0.001), Zn and albumin (r = 0.633, p < 0.001), and negative correlations between Fe and ferritin content (r = -0.521, p < 0.05) and Fe and Tf (r = -0.616, p < 0.01) in the patients group. Our findings demonstrated that plasma essential trace elements Se, Cu, and Fe change, but these changes might be dependent on acute-phase proteins, which were regulated as a part of defense strategies of the organism, induced by hormonelike substances.
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PMID:Essential trace elements selenium, zinc, copper, and iron concentrations and their related acute-phase proteins in patients with vivax malaria. 1611 42

Metabolic acidosis is associated with most severe malaria deaths in African children, and most deaths occur before maximum antimalarial action is achieved. Thus, specific acidosis treatment may reduce mortality. However, the underlying mechanisms remain poorly understood and no specific interventions have been developed. A detailed characterisation of this acidosis is critical in treatment development. We used the traditional and Stewart's approach to characterise acidosis in consecutive paediatric admissions for malaria and other acute non-surgical conditions to Kilifi District Hospital in Kenya. The overall acidosis prevalence was 21%. Gastroenteritis had the highest prevalence (61%). Both the mean albumin-corrected anion gap and the strong ion gap were high (>13 mmol/l and >0 mmol/l, respectively) in malaria, gastroenteritis, lower respiratory tract infection and malnutrition. Presence of salicylate in plasma was not associated with acidosis but was associated with signs of severe illness (odds ratio 2.11, 95% CI 1.1-4.2). In malaria, mean (95% CI) strong ion gap was 15 (14-7) mmol/l, and lactate, creatinine and inorganic phosphorous explained only approximately 40% of the variability in base excess (adjusted R2 = 0.397). Acidosis may be more common than previously recognised amongst paediatric admissions in Africa and is characterised by the presence of currently unidentified strong anions. In malaria, lactate and ketones, but not salicylate, are associated with acidosis. However, unidentified anions may be more important.
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PMID:Characterisation of metabolic acidosis in Kenyan children admitted to hospital for acute non-surgical conditions. 1625 25

Calcium and phosphate levels were investigated in 39 children with malaria (six severe and 33 uncomplicated) and in 39 healthy children. Hypocalcaemia (calcium <2.13 mmol/L, adjusted for albumin level) was detected in 23.1% of malaria cases and in 5.1% of controls, and hypophosphataemia (<1 mmol/L) in 38.5% of cases and in 15.4% of controls. Mean (SD) calcium levels in cases [2.26 (0/15)] were similar to those in controls [2.24 (0.12)]. In Nigerian children, hypocalcaemia and hypophosphataemia are associated with malaria.
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PMID:Calcium and phosphate levels in Nigerian children with malaria. 1629 6

Gateways to Clinical Trials are a guide to the most recent clinical trials in current literature and congresses. The data in the following tables have been retrieved from the Clinical Trials Knowledge Area of Prous Science Integrity, the drug discovery and development portal, http://integrity.prous.com. This issue focuses on the following selection of drugs: 131-I-chlorotoxin; Ad5CMV-p53, adalimumab, albumin interferon alfa, alemtuzumab, aliskiren fumarate, aminolevulinic acid methyl ester, anakinra, AR-C126532, atomoxetine hydrochloride; Bevacizumab, bosentan, botulinum toxin type B, brimonidine tartrate/timolol maleate; Calcipotriol/betamethasone dipropionate, cangrelor tetrasodium, cetuximab, ciclesonide, cinacalcet hydrochloride, collagen-PVP, Cypher; Darbepoetin alfa, darusentan, dasatinib, denosumab, desloratadine, dexosome vaccine (lung cancer), dexrazoxane, dextromethorphan/quinidine sulfate, duloxetine hydrochloride; ED-71, eel calcitonin, efalizumab, entecavir, etoricoxib; Falciparum merozoite protein-1/AS02A, fenretinide, fondaparinux sodium; gamma-Hydroxybutyrate sodium, gefitinib, ghrelin (human); hLM609; Icatibant acetate, imatinib mesylate, ipsapirone, irofulven; LBH-589, LE-AON, levocetirizine, LY-450139; Malaria vaccine, mapatumumab, motexafin gadolinium, muraglitazar, mycophenolic acid sodium salt; nab-paclitaxel, nelarabine; O6-Benzylguanine, olmesartan medoxomil, orbofiban acetate; Panitumumab, peginterferon alfa-2a, peginterferon alfa-2b, pemetrexed disodium, peptide YY3-36, pleconaril, prasterone, pregabalin; Ranolazine, rebimastat, recombinant malaria vaccine, rosuvastatin calcium; SQN-400; Taxus, tegaserod maleate, tenofovir disoproxil fumarate, teriparatide, troxacitabine; Valganciclovir hydrochloride, Val-Tyr sardine peptidase, VNP-40101M, vorinostat.
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PMID:Gateways to clinical trials. 1684 50

Liver function tests were performed in 61 vivax, 54 malariae and 15 ovale malaria patients who were admitted to Bangkok Hospital for Tropical Diseases between 2001 and 2004. The objective of the study was to evaluate changes in hepatic biochemical indices before and after treatment with artemisinin derivatives. On admission and prior to treatment, hepatic dysfunction was found among the 3 groups. Serum liver function tests and physical examinations were performed weekly during the 28-day follow-up period. Initially elevated serum bilirubin and diminished albumin returned to normal within 2 weeks of treatment. Serum alkaline phosphatase and aminotransferases returned to within normal limits within 3 weeks. We conclude that patients with Plasmodium vivax, P. malariae and P. ovale infections had slightly elevated serum bilirubin, aminotransferase and alkaline phosphatase levels, and hypoalbuminemia. These minor abnormalities returned to normal within a few weeks after treatment with therapies based on artemisinin derivatives.
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PMID:Minor liver profile dysfunctions in Plasmodium vivax, P. malaria and P. ovale patients and normalization after treatment. 1717 May 71

Gateways to Clinical Trials are a guide to the most recent clinical trials in current literature and congresses. The data in the following tables have been retrieved from the Clinical Trials Knowledge Area of Prous Science Integrity, the drug discovery and development portal, http://integrity.prous.com. This issue focuses on the following selection of drugs: 5-Methyltetrahydrofolate, 9-aminocamptothecin; AdPEDF.11, AE-37, albumin interferon alfa, alicaforsen sodium, alvocidib hydrochloride, AMG-706, arginine butyrate, avanafil, axitinib, azimilide hydrochloride; BAY-579352, belagenpumatucel-L, beta-lapachone, BHT-3009, BIBW-2992, bremelanotide, BX-471; Casopitant mesylate, cediranib, certolizumab pegol, CH-1504, ChimeriVax-West Nile, clofazimine, CpG-7909, curcumin, Cypher; Dapoxetine hydrochloride, darusentan, diflomotecan, D-methionine, dnaJP1, D-serine, DTPw-HB Hib-MenAC, DTPw-HepB-Hib; E-7010, ecogramostim, edodekin alfa, EGFRvlll peptide vaccine, elcometrine, elcometrine/ethinylestradiol, elsilimomab, enrasentan, ertumaxomab, etalocib sodium, exisulind; Fenretinide, fesoterodine, fingolimod hydrochloride, fontolizumab; Gefitinib, gemtuzumab ozogamicin, ghrelin (human), GV-1001; HTU-PA, human papillomavirus vaccine; Indacaterol, indiplon, interleukin-21, intranasal insulin, irinotecan hydrochloride/floxuridine, ISIS-301012, ispinesib mesylate, ixabepilone; K562/GM-CSF; Lapatinib, L-BLP-25, linezolid, liposome encapsulated paclitaxel, LY-2124275; MC-1, MC-1/lisinopril, MDX-066, melanoma vaccine, MMR-V, multivalent (ACYW) meningitis vaccine; Nilotinib, nobori, nociceptin; Oblimersen sodium, orbofiban acetate, ospemifene; Paliperidone, panitumumab, PEG-filgrastim, PEGylated interferon alfacon-1, perflubutane, pertuzumab, phenserine tartrate, phVEGF-A165, pleconaril, prasugrel, prednisolone sodium metasulfobenzoate; R-411, recombinant malaria vaccine, rhGM-CSF, roflumilast, romidepsin, ruboxistaurin mesilate hydrate; Sirolimus-eluting stent, SR-4554, St. John's Wort extract; Talabostat, Taxus, TGN-255, tifacogin, tiotropium bromide, tolevamer sodium, trabectedin, tretinoin LF; Vatalanib succinate; Yellow fever vaccine, YM-155.
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PMID:Gateways to clinical trials. 1723 18

Rosetting of Plasmodium falciparum-infected red blood cells (parasitized RBC [pRBC]) with uninfected RBC has been associated in many studies with malaria morbidity and is one form of cytoadherence observed with malarial parasites. Rosetting is serum dependent for many isolates of P. falciparum, including the strains FCR3S1.2 and Malayan Camp studied here. We identified the three naturally occurring components of sera which confer rosetting. Complement factor D alone induced 30 to 40% of de novo rosetting. Its effect was additive to that of 0.5 mg/ml albumin and to that of 15 ng/ml of naturally occurring antibodies to the anion transport protein, band 3. The three components together mediated rosetting as effectively as 10% serum. De novo rosetting experiments showed that naturally occurring anti-band 3 antibodies as well as factor D were effective only when added to pRBC. Factor D appeared to cleave a small fraction of a protein expressed on the surface of pRBC.
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PMID:Complement factor D, albumin, and immunoglobulin G anti-band 3 protein antibodies mimic serum in promoting rosetting of malaria-infected red blood cells. 1726 5

The virulence of the malaria parasite Plasmodium falciparum is related to its ability to express a family of adhesive proteins known as P. falciparum erythrocyte membrane protein 1 (PfEMP1) at the infected red blood cell surface. The mechanism for the transport and delivery of these adhesins to the erythrocyte membrane is only poorly understood. In this work, we have used specific immune reagents in a flow cytometric assay to monitor the effects of serum components on the surface presentation of PfEMP1. We show that efficient presentation of the A4 and VAR2CSA variants of PfEMP1 is dependent on the presence of serum in the bathing medium during parasite maturation. Lipid-loaded albumin supports parasite growth but allows much less efficient presentation of PfEMP1 at the red blood cell surface. Analysis of the serum components reveals that lipoproteins, especially those of the low-density lipoprotein fraction, promote PfEMP1 presentation. Cytoadhesion of infected erythrocytes to the host cell receptors CD36 and ICAM-1 is also decreased in infected erythrocytes cultured in the absence of serum. The defect appears to be in the transfer of PfEMP1 from parasite-derived structures known as the Maurer's clefts to the erythrocyte membrane or in surface conformation rather than a down-regulation or switching of particular PfEMP1 variants.
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PMID:Serum lipoproteins promote efficient presentation of the malaria virulence protein PfEMP1 at the erythrocyte surface. 1764 56


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